Reversal of cell polarity and actin-myosin cytoskeleton reorganization under mechanical and chemical stimulation

Reversal of cell polarity and actin-myosin cytoskeleton reorganization under mechanical and chemical stimulation
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DOI:
10.1529/biophysj.107.114702
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发表时间:
2008-02-01
影响因子:
3.4
通讯作者:
Bretschneider, Till
Bretschneider, Till
中科院分区:
生物学3区
文献类型:
--
作者:
Dalous, Jeremie;Burghardt, Emmanuel;Bretschneider, Till

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为了研究细胞中肌动蛋白系统极性反转的重组,我们用交替方向的机械力刺激盘形骨细胞。通过建立一个朝向流动的突出的前部和一个收缩的尾部来在流体流动中定向的细胞。标记聚合肌动蛋白和。前尾部有肌球蛋白- II标记。在2.1 Pa时,肌动蛋白首先在先前的前沿分解,然后在新诱导的前沿开始聚合。相反,肌球蛋白- ii从前一条尾巴上慢慢消失,并不断地重新分布到新尾巴上。前部规格与肌球蛋白- ii无关,聚合肌动蛋白的积累在缺乏肌球蛋白- ii重链的突变体中更加集中。我们得出的结论是,在机械刺激下,细胞极性反转是由一个全局的内部信号启动的,该信号抑制了整个细胞中的肌动蛋白聚合。它被认为是在细胞最强烈的刺激部位,即早期的前部区域被激发,并被一个缓慢产生的短距离信号所抵消,该信号局部激活前部的肌动蛋白聚合。在化学引诱剂环状AMP的强梯度下,细胞重定向时也观察到类似的前后相互转换模式。
To study reorganization of the actin system in cells that invert their polarity, we stimulated Dictyostelium cells by mechanical forces from alternating directions. The cells oriented in a fluid flow by establishing a protruding front directed against the flow and a retracting tail. Labels for polymerized actin and. lamentous myosin- II marked front and tail. At 2.1 Pa, actin first disassembled at the previous front before it began to polymerize at the newly induced front. In contrast, myosin-II slowly disappeared from the previous tail and continuously redistributed to the new tail. Front specification was myosin-II independent and accumulation of polymerized actin was even more focused in mutants lacking myosin-II heavy chains. We conclude that under mechanical stimulation, the inversion of cell polarity is initiated by a global internal signal that turns down actin polymerization in the entire cell. It is thought to be elicited at the most strongly stimulated site of the cell, the incipient front region, and to be counterbalanced by a slowly generated, short- range signal that locally activates actin polymerization at the front. Similar pattern of front and tail interconversion were observed in cells reorienting in strong gradients of the chemoattractant cyclic AMP.